Field of the Invention
The present invention relates generally to the fields of molecular biology and medicine. More particularly, it concerns therapeutic peptides.
Description of Related Art
Age-related macular degeneration (AMD) is a progressive multifactorial disease involving genetic abnormalities and environmental insults. It is the leading cause of blindness for Americans over sixty. Dry AMD is characterized by drusen, retinal pigment epithelia (RPE) damage, and photoreceptor loss. In wet AMD, which develops from dry AMD, subsequent pathological events include breakdown of RPE/Bruch's membrane, increased release of the pro-angiogenic factor VEGF and development of choroidal neovascularization (CNV). Intact tight-junctions have been shown to be essential for efficient removal of fluid from the subretinal space and for barrier function of the RPE. Subretinal fluid accumulation has been reported in AMD, implying impaired barrier function. Barrier properties rely on tight junctions (TJ), which are protein complexes (including claudin, occludin, Jam) that link via the zonula occludens (ZO-1) protein to the actin cytoskeleton. ZO-1 is believed to form a scaffold at the face of the junction, and ZO-1 may function as a key cytoplasmic regulator of TJ stability.
Treatment options for AMD are currently limited. VEGF blocking therapies are often used to treat wet AMD; however, such therapies present various limitations. For example, VEGF treatment typically involves repeated intravitreal injections and is FDA-limited to 2-years, as side effects from repeat injections might outweigh treatment benefit.
Injuries and inflammation resulting from trauma, surgery, or disease continues to be a problem. Clearly, there is a need for new therapies to promote wound healing and/or decrease inflammation.